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Sediments deposited from the Permian–Triassic boundary (~252 Ma) until the end-Smithian (Early Triassic; c. 250.7 Ma) in the Sonoma Foreland Basin show marked thickness variations between its southern (up to c. 250 m thick) and northern (up to c. 550 m thick) parts. This basin formed as a flexural response to the emplacement of the Golconda Allochthon during the Sonoma orogeny. Using a high-resolution backstripping approach, a numerical model and sediment thickness to obtain a quantitative subsidence analysis, we discuss the controlling factor(s) responsible for spatial variations in thickness. We show that sedimentary overload is not sufficient to explain the significant discrepancy observed in the sedimentary record of the basin. We argue that the inherited rheological properties of the basement terranes and spatial heterogeneity of the allochthon are of paramount importance in controlling the subsidence and thickness spatial distribution across the Sonoma Foreland Basin.

Moderate ethanol drinking (ED) and n-3 fatty acids have both been associated with low cardiac mortality. However, there are few data evaluating the interactions of ED with n-3. We recently reported that moderate ED results in increased n-3 in cardiac patients. The main aim of the present study was, through a well-controlled experimental model, to confirm that chronic ED actually results in increased n-3. Secondary aims were to examine the effects of chronic ED on cardiac mitochondria, cardiac function and experimental myocardial infarction. We studied the fatty acid profiles of plasma, cell membranes and cardiac mitochondria phospholipids in a rat model of chronic ED. In plasma and cell membranes, ED actually resulted in higher n-3 (P = 0·005). In mitochondria phospholipids of ED rats, n-3 were also increased (P < 0·05) but quite modestly. Cardiac mitochondrial function and left ventricular function were not significantly different in ED and control rats, while infarct size after 30 min ischaemia and reperfusion was smaller (P < 0·0001) in ED rats. This is the first animal study confirming interaction of alcohol drinking with n-3. We found no harmful effect of chronic ED on the heart in that model but a significant cardioprotection. Further studies are warranted to investigate the mechanisms by which moderate ED alters the metabolism of n-3 and whether n-3 are the mediators of the ED-induced cardioprotection.

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